Kidney Stones

Urinary tract stone disease is one of the most painful diseases endured by humans for centuries. The reference of the disease dates back to Egyptian Mummies with several medicals records cited as evidence.

Kidney stone, also called as renal colic, is a solid crystalline mass found within the kidney or the urinary tract. Acute renal colic is one of the worst pains a person can endure and affects approximately millions of people each year.

If the crystals formed are tiny enough, it will pass out of the body through the urine stream. However, large crystals may cause obstruction and pain in the flow of urine and requires non-surgical or surgical intervention.

Urinary tract stone disease is caused by two basic phenomena:

The first phenomenon is supersaturation of the urine by stone-forming constituents, including calcium, oxalate, and uric acid. Crystals or foreign bodies can build up within the ureter to form microscopic crystalline structures, causing pain as they pass towards the urinary bladder. A major portion of these tiny crystals constitutes of calcium. Uric acid calculi and crystals of uric acid comprise the remaining minority. Other, less frequent stone types include cystine, ammonium acid urate, xanthine, dihydroxyadenine, and various rare stones related to precipitation of medications in the urinary tract.

The second phenomenon, which is most likely responsible for calcium oxalate stones, is deposition of stone material on a renal papillary calcium phosphate nidus, typically a Randall plaque (which is always composed of calcium phosphate). Calcium phosphate precipitates in the basement membrane of the thin loops of Henle, erodes into the interstitium, and then accumulates in the subepithelial space of the renal papilla. The subepithelial deposits, which have long been known as Randall plaques, eventually erode through the papillary urothelium. Stone matrix, calcium phosphate, and calcium oxalate gradually deposit on the substrate to create a urinary calculus.

Urinary stone disease can be attributed to low fluid intake with subsequent low volume of urine productions which results in formation of crystals in the urine. Hypercalciuria, related to increased intestinal absorption of calcium due to excess dietary calcium absorption and hyperparathyroidism, characterized by excess calcium resorption from bone, can cause urinary stone. A decreased level of magnesium and citrate in the urine also causes stone formation.

The four main types of renal calculi are described below:

Calcium StonesAround 75% of renal calculi are caused due to calcium stones. In Hypercalciuric patients, a low-protein, low salt diet may be preferable to a low calcium diet to prevent stone recurrences. Studies have shown that incidence of stone formation is inversely proportional to dietary calcium intake. A trend followed in urology does not suggest restriction of dietary intake of calcium, a very important factor for postmenopausal women who are in risk of osteoporosis. Calcium oxalate, calcium phosphate, and calcium urate are associated with the following disorders:

Increased gut absorption of calcium – It is the most common cause of hypercalciuria, treated with calcium binders or thiazides plus potassium citrate

Uric acid stonesAbout 6% of renal calculi are due to Uric acid stones. Urine pH is less than 5.5. These stones results from high purine intake (eg, organ meats, legumes, fish, meat extracts, gravies), or malignancy (ie, rapid cell turnover). Approximately 25% of patients are affected due to condition such as gout. Serum and 24-hour urine sample should be sent for creatinine and uric acid determination. If serum or urinary uric acid is elevated, the patient may be treated with allopurinol 300 mg daily. Patients with normal serum or urinary uric acid are best managed by alkali therapy alone.

Cystine stones Cystine stones account for 2% of renal calculi. This is a hereditary condition which arises due to intrinsic metabolic defect resulting in failure of renal tubular reabsorption of cystine, ornithine, lysine, and arginine. Urine becomes supersaturated with cystine, with resultant crystal deposition.

The morbidity of urinary tract calculi is due to obstruction with acute pain. Nonobstructing calculi may not cause acute pain but may produce considerable discomfort. Serious complications of urinary tract stone disease include the following:

Abscess formation

Serious infection of the kidney that diminishes renal function

Urinary fistula formation

Ureteral scarring and stenosis

Ureteral perforation

Extravasation

Urosepsis

Renal loss due to long-standing obstruction

Infected hydronephrosis is the most deadly complication related to urinary stone disease because infection adjacent to the highly vascular renal parenchyma places the patient at risk for rapidly progressive sepsis and death. A ureteral stone associated with obstruction and upper UTI is a high risk factor. Immediate involvement of the urologist is essential. Calyceal rupture with perinephric urine extravasation due to high intracaliceal pressures occasionally is seen and usually is treated conservatively. Complete ureteral obstruction may occur in patients with tightly impacted stones. This is best diagnosed via IVP and is not discernible on noncontrast CT scan. Patients with 2 healthy kidneys can tolerate several days of complete unilateral ureteral obstruction without long-term effects on the obstructed kidney. If a patient with complete obstruction is well hydrated and pain and vomiting are well controlled, the patient can be discharged from the ED with urologic follow-up within 1-2 days.

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Symptoms of urinary stone disease may include pain, infection, or hematuria. Small nonobstructive stones in the kidney may only cause occasional pain and can be easily controlled. The passage of stones into the ureter with acute obstruction, proximal urinary tract dilation, and spasm is associated with classic renal colic. Acute pain radiating to the groin with nausea and vomiting may indicate renal colic caused by an acute ureteral renal pelvic obstruction. Renal colic without obstruction rarely pain.

Patients with large renal stones known as staghorn calculi are often relatively asymptomatic. The term "staghorn" refers to the presence of a branched kidney stone occupying the renal pelvis and at least one calyceal system. Such calculi usually manifest as infection and hematuria rather than as acute pain. Asymptomatic bilateral obstruction, which is uncommon, manifests as symptoms of renal failure. Important historical features related to analysis of urinary stone disease are as follows:

Duration, characteristics, and location of pain

History of urinary calculi

Prior complications related to stone manipulation

Urinary tract infections

Loss of renal function

Family history of calculi

Solitary or transplanted kidney

Chemical composition of previously passed stones

Location and characteristics of pain is a very important factor in determining urinary stone disease. Most calculi originate within the kidney, creating urinary obstruction as they proceed and become lodged in narrow areas including the ureteropelvic junction, pelvic brim, and ureterovesical junction. Location and quality of pain are associated with the position of the stone within the urinary tract. Severity of pain is related to the degree of obstruction, presence of ureteral spasm, and presence of any associated infection.

Stones obstructing the ureteropelvic junction may cause mild-to-severe deep flank pain without radiation to the groin, due to distention of the renal capsule. Stones impacted within the ureter cause abrupt, severe pain in the flank and ipsilateral lower abdomen with radiation to the testicles or the vulvar area. Intense nausea, with or without vomiting, usually is present.

Pain from upper ureteral stones tends to radiate to the flank and lumbar areas. On the right side, this can be confused with cholecystitis or cholelithiasis; on the left, the differential diagnoses include acute pancreatitis, peptic ulcer disease, and gastritis. Midureteral calculi cause pain that radiates anteriorly and caudally. This midureteral pain in particular can easily mimic appendicitis on the right or acute diverticulitis on the left.

Distal ureteral stones cause pain that tends to radiate into the groin or testicle in the male or labia majora in the female because the pain is referred from the ilioinguinal or genitofemoral nerves.

Stones present in the ureterovesical junction may cause irritative voiding symptoms, such as urinary frequency and dysuria. If a stone is lodged in the intramural ureter, symptoms may appear similar to cystitis or urethritis. These symptoms include suprapubic pain, urinary frequency, urgency, dysuria, stranguria, pain at the tip of the penis, and sometimes various bowel symptoms, such as diarrhea and tenesmus. These symptoms can be confused with pelvic inflammatory disease, ovarian cyst rupture, or torsion and menstrual pain in women. Calculi that have entered the bladder are usually asymptomatic and are passed relatively easily during urination. Rarely, a patient reports positional urinary retention (obstruction precipitated by standing, relieved by recumbency), which is due to the ball-valve effect of a large stone located at the bladder outlet.

Other symptoms of urinary stone disease may include nausea and vomiting in at least 50% of patients with acute renal colic. Nausea is caused by the common innervation pathway of the renal pelvis, stomach, and intestines through the celiac axis and vagal nerve afferents. This is often compounded by the effects of narcotic analgesics, which often induce nausea and vomiting through a direct effect on gastrointestinal (GI) motility and an indirect effect on the chemoreceptor trigger zone in the medulla oblongata. Nonsteroidal anti-inflammatory drugs (NSAIDs) can often cause gastric irritation and GI upset. The presence of a renal or ureteral calculus is not a guarantee that the patient does not have some other, unrelated medical problem causing the GI symptoms.

In some cases, a stone may pass before the definitive imaging procedure has been completed. In these cases, residual inflammation and edema still may cause some transient or diminishing obstruction and pain even without any stone being positively identified.

UrinalysisPatients suspected of having renal colic, microscopic examination of the urine for evidence of hematuria and infection becomes a critical part of the evaluation process. Gross or microscopic hematuria is present in approximately 85% of patients with urinary calculi. However, lack of microscopic hematuria does not eliminate the risk of renal colic. Attention should also be paid to the presence or absence of leukocytes, crystals, and bacteria and to the urinary pH level. In general, if the number of white blood cells (WBCs) in the urine is greater than 10 cells per high-power field or greater than the number of RBCs, UTI can be suspected. Pyuria (>5 WBCs/hpf on a centrifuged specimen) in a patient with ureterolithiasis should prompt a careful search for signs of infected hydronephrosis.

Urinary crystals of calcium oxalate, uric acid, or cystine may occasionally be found upon urinalysis. Presence of these crystals gives a clue about the nature and type of obstructing calculus. Also, a urine pH greater than 7 suggests presence of urea-splitting organisms, such as Proteus, Pseudomonas, or Klebsiella species, and struvite stones. A urine pH less than 5 suggests uric acid stones.

Blood Studies

A patient with acute kidney stone attack may have renal infection accompanied by serum WBC count of 15,000/µL or higher. Mild leukocytosis often accompanies a renal colic attack. A depressed RBC count suggests a chronic disease state or severe ongoing hematuria.

To assess a patient’s current renal health and to diagnose metabolic risk of future stone formation, measurements of serum electrolyte, creatinine, calcium, uric acid, parathyroid hormone (PTH), and phosphorus are essential. A high serum uric acid level may indicate gouty diathesis or hyperuricosuria, while hypercalcemia suggests either renal-leak hypercalciuria (with secondary hyperparathyroidism) or primary hyperparathyroidism. If the serum calcium level is elevated, serum PTH levels should be obtained.

Serum creatinine level is the major predictor of contrast-induced nephrotoxicity. If the creatinine level is higher than 2 mg/dL, diagnostic techniques should be used that do not require an infusion of contrast, such as ultrasonography or helical CT scanning.

24-Hour Urine Profile A 24-hour urine profile with appropriate serum tests of renal function, uric acid, and calcium can identify any associated urinary stone disease. The test can identify the exact nature of the chemical problem that caused stone formation. The tests can also reveal any other significant health problem the patient may have. A 24-hour urinalysis may indicate the following objectives:

Residual calculi after surgical treatment

Initial presentation with multiple calculi

Initial presentation before age 30 years

Renal failure

Solitary kidney (including renal transplant)

Family history of calculi

More than 1 stone in the past year

Bilateral calculi

It is very important to consider patient’s preference to perform a 24-hour urine study. If the patient is willing to follow a protracted stone-prevention treatment plan involving diet, supplements, medications, a 24-hours urine study can be obtained. In case, the patient is not willing to follow a long-term plan, the patient can be counseled to make them understand about the importance of treatment and that without proper treatment they will be prone to frequent calculi formation.

The most common findings on 24-hour urine studies include hypercalciuria, hyperoxaluria, hyperuricosuria, hypocitraturia, and low urinary volume. Other factors, such as high urinary sodium and low urinary magnesium concentrations, may also play a role. A finding of hypercalcemia should prompt follow-up with an intact parathyroid hormone study to evaluate for primary and secondary hyperparathyroidism.

Elevation of the 24-hour excretion rate of calcium, oxalate, or uric acid indicates a risk factor of forming calculi. Hypercalciuria can be subdivided into absorptive, resorptive, and renal-leak categories on the basis of the results of blood tests and 24-hour urinalysis on both regular and calcium-restricted diets. Depending on the specific subtype, the treatment of absorptive hypercalciuria may include dietary calcium restriction, thiazide diuretics, oral calcium binders, or phosphate supplementation. Resorptive hypercalciuria is primary hyperparathyroidism and requires parathyroidectomy, when possible. In case, parathyroid surgery is not possible, phosphate supplementation is usually recommended. Renal-leak hypercalciuria, which is less common than absorptive hypercalciuria, is usually associated with secondary hyperparathyroidism and is best managed with thiazide diuretics.

Excess sodium excretion can contribute to hypercalciuria by a phenomenon known as solute drag. Elevated urinary sodium levels are almost always associated with dietary indiscretions. A decrease in oral sodium intake can decrease calcium excretion thus causing decrease calcium saturation. An elevated phosphorus level is useful as a marker for a subtype of absorptive hypercalciuria known as renal phosphate leak (absorptive hypercalciuria type III). Renal phosphate leak is identified by high urinary phosphate levels, low serum phosphate levels, high serum level of 1,25 vitamin D-3 (calcitriol), and hypercalciuria. This type of hypercalciuria is uncommon and does not respond well to standard therapies.

The above laboratory tests are confirmatory but are performed only if the index of clinical suspicion is high. Any patient with hypercalciuria who has a low serum phosphorus level and a high-normal or high urinary phosphorus level may have this condition. Repeated laboratory tests along with a 1,25 vitamin D-3 level can be a confirmation. Phosphate supplements are used to correct the low serum phosphate level, which then decreases the inappropriate activation of vitamin D originally caused by the hypophosphatemia. This corrects the hypercalciuria, which is ultimately a vitamin D–dependent function in this condition. However, this therapy may not be well tolerated.

Magnesium and citrate are important chemical inhibitors of stone formation. Hypocitraturia is one of the most common metabolic defects that predispose to stone formation. Citrate therapy is recommended as primary or adjunctive therapy who have formed recurrent calcium-containing stones. Many laboratories use 24-hour urine citrate levels of 320 mg/d as the normal threshold, but optimal levels are probably closer to the median level (640 mg/d) in healthy individuals. Periodic monitoring of pH with pH test strips can be very useful to titrate and optimize citrate supplementation. A pH level of 6.5 is usually considered optimal. A pH level over 7.0 should be discouraged, as it prompts calcium phosphate precipitation.

Creatinine is the control that allows verification of a true 24-hour sample. Most individuals excrete 1-1.5 g of creatinine daily. Values at either extreme that are not explained by estimates of lean body weight should prompt consideration that the sample is inaccurate.

Plain (KUB) RadiographyPlain abdominal radiography (also referred to as KUB radiography) is useful for assessing total stone burden, as well as the size, shape, composition, and location of urinary calculi in some patients. If a stone is not visible on a flat plate radiograph, it could be a radiolucent uric acid stone that can be dissolved with alkalinizing medication. Such a stone is more likely if the urine pH indicates very acidic urine. In practice, any patient with symptoms of acute renal colic who demonstrates a urine pH lower than 6.0 should be considered at risk for a possible uric acid stone. If a stone of adequate size is visible on a CT scan but not visible on KUB, then uric stones should be considered.

The primary advantage of flat plate radiograph is that it is inexpensive, quick, and usually helpful even if no specific stone is observed. The progress of the stone can be easily monitored with a follow-up KUB radiograph, which may prove helpful in determining the exact size and shape of the stone, in establishing a baseline for follow-up studies, and for visualization of the surgical orientation.

Disadvantage may involve a relatively low sensitivity (40-50%) and specificity for renal and ureteral calculi. Any calcific density observed on a KUB radiograph that happens to overlie the course of the ureter is not guaranteed to be a stone.

UltrasonographyRenal ultrasonography can be used to determine the presence of a renal stone. A stone easily identified with renal ultrasonography but not visible on the plain radiograph may be a uric acid or cystine stone, which is potentially dissolvable with urinary alkalinization therapy. For some stones, ultrasonography works quite well; however, it has been found to be less accurate in diagnosis of ureteral stones especially those in the distal ureter, than IVP or CT. Diagnostic criteria include direct visualization of the stone, hydroureter more than 6 mm in diameter, and perirenal urinoma suggesting calyceal rupture. Also, ultrasonography is not reliable for small stones (ie, those smaller than 5 mm) and does not help in the evaluation of kidney function. Ultrasonography requires no intravenous (IV) contrast and can easily detect any significant hydronephrosis. Renal ultrasonography works best in the setting of relatively large stones within the renal pelvis or kidney.

Intravenous Pyelography (Urography)IVP, also known as intravenous urography (IVU), was used in diagnosing ureterolithiasis. IVP provides a clear outlone of the entire urinary system making visualization of even mild hydronephrosis relatively easy. IVP is helpful in identifying the specific problematic stone among numerous pelvic calcifications, as well as in demonstrating renal function and establishing that the other kidney is functional. These determinations are particularly helpful if the degree of hydronephrosis is mild and the noncontrast CT scan findings are not definitive. IVP can also show nonopaque stones as filling defects.

Disadvantages include the need for IV contrast material, which may provoke an allergic response or renal failure, and the need for multiple delayed films, which can take up to 6 hours. Obtaining the IVP is also a relative labor-intensive process. In addition, IVP may fail to reveal alternative pathology if a stone is not discovered, delaying the final diagnosis. False-negative results usually occur with stones located at the ureterovesical junction.

Computed Tomography ScanningCT scan is used in the assessment of urinary tract stone disease, especially in case of acute renal colic. CT scans are readily available in most hospitals and can be performed and read in just a few minutes. Numerous studies have demonstrated that CT has a sensitivity of 95-100% and superior specificity and accuracy when compared with IVP. A renal colic study consists of a noncontrast or unenhanced CT scan of the abdomen and pelvis, including very narrow cuts taken through the kidneys and bladder areas, where symptomatic stones are most likely to be encountered.

Advantages of CT scanning include the following:

It can reveal other pathology like appendicitis, pancreatitis, cholecystis, ovarian disorders, diverticular disease, renal carcinoma, which is helpful in case the patient’s true underlying pathology is something other than a kidney stone.

It can be performed very quickly in less than five minutes

It avoids the use of IV contrast materials.

The density of the stone can assist in predicting stone composition and response to shockwave lithotripsy.

Disadvantages of CT scanning involve:

It cannot be used to assess individual renal function or degree of obstruction.

It can fail to reveal some unusual radiolucent stones, such as those caused by indinavir and atazanavir, which are typically invisible on the CT scan.

Sulfadiazine stones are also difficult to visualize on CT because of relatively low attenuation.

It is relatively expensive.

It exposes the patient to a relatively high radiation dose (and thus should not be performed on pregnant women).

Precise identification of small distal stones is occasionally difficult.

Stone size as measured on CT KUB correlates poorly with actual size of the stone measured after spontaneous passage. For this reason, caution should be used in counseling patients on the likelihood of spontaneous stone passage when stone size is determined using CT-based measurement.

Although CT scans can be used to estimate the overall size, width, and location of a stone, they can only approximate its shape. Stone location can be described in anatomical terms, but the CT scan lacks the surgical orientation that most urologists prefer.

If a KUB or flat plate radiograph is performed at the same time as the CT scan, some of these objections and problems disappear. However, obtaining the extra films involves some additional delay, the patient is exposed to more ionizing radiation, and the total cost for the workup increases. The "scout" reconstruction of the CT scan, formatted to look like a plain radiograph, can be substituted for a formal KUB radiograph in certain cases. Stones of size 3 mm or more can be identified though these studies.

Retrograde PyelographyRetrograde Pyelography is the most precise imaging method for determining the anatomy of the ureter and renal pelvis for making a definitive diagnosis of any ureteral calculus. In this, the patient is taken to the operating room (OR) cystoscopy suite and an endoscopic examination is performed with the patient under anesthesia. After a cystoscope is placed in the bladder, a thin ureteral catheter is inserted into the ureteral orifice on the affected side. A radiographic picture is taken while contrast material is injected through the ureteral catheter directly into the ureter. Any stone, even if radiolucent, and any ureteral kinks, strictures, or tortuousities that may not be visualized easily on other studies become clearly visible. Retrograde pyelograms are performed when a precise diagnosis cannot be obtained by other means. They are considered essential when surgery is deemed necessary because of uncontrollable pain, severe urinary infection or urosepsis with a blocked kidney, a solitary obstructed kidney, a stone that is considered unlikely to pass spontaneously because of its large size (generally ≥8 mm), or the presence of possible anatomical abnormalities (eg, ureteral strictures).

Retrograde pyelograms can be performed safely both in patients highly allergic to IV contrast media and in patients with renal failure because the contrast medium never enters the bloodstream and therefore requires no renal filtration or excretion and causes no anaphylaxis.

Nuclear Renal ScanningA nuclear renal scan can be used to measure differential renal function, especially in a dilated system for which the degree of obstruction is in question. This is also a reasonable study in pregnant patients, in whom radiation exposure must be limited.

The intravenously injected radioisotope is eliminated via the nephron, with the rate of clearance from the renal unit providing an excellent estimate of the glomerular filtration rate and the relative rate of drainage or clearing from each kidney. A drainage half-time that is 20 minutes or longer indicates obstruction, while a drainage half-time of 10 minutes or less is considered unobstructed. If the drainage half-time is 10-20 minutes, the result is indeterminate.

Magnetic Resonance Imaging In most cases, direct detection of most stones is not possible with MRI, and MRI should not be used for that purpose in most instances. MRIs are generally more expensive than other studies, such as CT scans, which reveal stones much better.

Since, MRI produces no dangerous radiation, the gadolinium contrast it uses has minimal nephrotoxicity, and it can readily reveal urinary obstruction even if the stones themselves are not easily visualized, MRI scanning is used in selected cases in which other technologies are too toxic or potentially dangerous. However, use of MRI in pregnant patients is somewhat controversial. Long-term effects on the fetus are unknown, and MRI is not specifically indicated in pregnancy.

Treatment of urinary stone disease involves emergency management of renal (ureteral) colic, with or without surgical interventions and medical therapy. In case of an emergency situation, the focus of the treatment should be in correcting dehydration, treating urinary infections and reducing risk of acute renal failure. Intravenous (IV) hydration can be provided to control nausea and vomiting.

For long term nephrolithiasis prophylaxis, a stone chemical composition analysis should be performed and information should be provided to motivated patients about possible 24-hour urine testing. Another important aspect of treatment is the size of the stone. Smaller stone, less than 4 mm in diameter has an 80% chance of spontaneous passage while stones larger than 8 mm in diameter have a 20% chance. Apart from the size, the shape and location of the stone and the specific anatomy of the upper urinary tract is of equal importance. In case of pregnancy for mild to moderate pain, acetaminophen can be monitored. Opioid drugs, such as morphine and meperidine, are a pregnancy category C medication, which can be used. However, Opioids can cause respiratory depression in the fetus; therefore, they should not be used near delivery or when other medications are adequate.

Medical therapy for urinary stone disease involves both short term and long term plan. The short term plan includes measures to dissolve the stone or facilitate stone passage. Long term plan includes treatment to prevent formation of stones in future. Long term treatment plan is advisable in case of stone formation before the age of 30, family history and residual stones after surgical treatment.

Hospital admission is necessary in case of acute renal colic syndrome. In most cases, patients recover sufficiently to go home within 24 hours. If at all hospitalization is required, it is for an observation. Patients can be hospitalized in case:

Oral analgesics becomes insufficient to manage pain

Ureteral obstruction from a stone occurs in a solitary or transplanted kidney.

Ureteral obstruction from a stone occurs in the presence of a urinary tract infection (UTI), fever, sepsis, or pyonephrosis.

Once renal (ureteral) colic is diagnosed, the next step is to determine the presence or absence of obstruction or infection in urine. If there is obstruction without infection, it can be managed with analgesics and other medical measures to facilitate the passage of stone through urine. In case of infection without obstruction, antimicrobial therapy can be used. However, if neither obstruction nor infection is present, analgesics and other medical measures can be employed to facilitate passage of the stone with the expectation that the stone will likely pass from the upper urinary tract if its diameter is smaller than 5-6 mm. Stones, larger in size, will require surgical intervention. In case of both obstruction and infection emergency decompression of the upper urinary collecting system is required.

Pain reliefUrinary stone pain can be managed with the usage of analgesia which can be achieved with parenteral narcotics or nonsteroidal anti-inflammatory drugs (NSAIDs). If the patient can tolerate oral intake of drugs, a combination of oral narcotics, NSAIDs, and antiemetics, can be used as an approach for renal (ureteral) colic.

Parenteral narcotics work primarily on the central nervous system (CNS) to reduce the perception of pain. They are inexpensive and quite effective. The most commonly used agent includes morphine, meperidine, and butorphanol. However, the choice of the agent is completely arbitrary. The usual dosage is 10 mg/70 kg body weight intramuscularly (IM) or subcutaneously (SC) every 4 hours. The actual dosage of the drug varies as per patient’s tolerance and severity or discomfort. For more rapid results, morphine sulfate can be administered IV in doses of 4-10 mg, but this must be done slowly or in small increments to avoid excessive adverse effects.

Adverse effects of morphine include respiratory depression, drowsiness, mood changes, nausea, vomiting, increases in the cerebrospinal fluid pressure, and cough reflex depression. Ketorolac works at the peripheral site of pain production rather than on the CNS. It has been proven in multiple studies to be as effective as opioid analgesics, with fewer adverse effects. The dosage is 30-60 mg IM or 30 mg IV initially followed by 30 mg IV or IM every 6-8 hours. A dose of 15 mg is recommended in patients older than 65 years.

Antiemetic therapy Antiemetic plays an important role in renal colic therapy because of the sedating effect that it creates because of nausea and vomiting associated with acute renal colic. The only antiemetic which has been specifically studied for the treatment of renal colic is metoclopramide reliving nausea. Its antiemetic effect stems from its dopaminergic receptor blockage in the CNS. It has no anxiolytic activity and is less sedating than other centrally acting dopamine antagonists. The effect of metoclopramide begins within 3 minutes of an IV injection, but it may not take effect for as long as 15 minutes if administered IM. The usual dose in adults is 10 mg IV or IM every 4-6 hours as needed. Metoclopramide is not available as a suppository. Other medications commonly used as antiemetics include promethazine, prochlorperazine, and hydroxyzine.

Active medical expulsive therapy Medical expulsive therapy (MET), is a more aggressive treatment approach. Studies have confirmed the efficacy of MET in reducing the pain of stone passage, increasing the frequency of stone passage, and reducing the need for surgery. MET is most useful in case of obstructive passage for stones 3-10 mm in size. MET is associated with a 65% greater likelihood of stone passage. The initially popularized regimens for MET included corticosteroids such as prednisone, as in the following example:

Limit MET to a 10- to 14-day course, as most stones that pass during this regimen do so in that time frame.

Surgical Care Surgical care is necessary in case of stones larger than 8 mm and is unlikely to pass spontaneously. Surgical intervention is of prime importance in case of acute pain, infection and obstruction. Infection associated with obstruction is a life threatening situation and must be treated as an emergency. Factors that promote surgical intervention includes:

Active, untreated UTI

Uncorrected bleeding diathesis

Pregnancy (a relative, but not absolute, contraindication)

Surgical interventional procedure can be accomplished by ureteral stent placement (a small tube placed endoscopically into the entire length of the ureter from the kidney to the bladder) or by percutaneous nephrostomy (a small tube placed through the skin of the flank directly into the kidney).

Stent placement Internal ureteral stents is a thin tube inserted in the ureter for treating obstructive urine flow. Stents are available in lengths from 20-30 cm and in 3 widths from 4.6F to 8.5F. Some stents are designed to soften up after placing it in the body, while others are stiff enough to resist from being crushed by large stones. The optimal stent width depends on both the relative diameter and course of the ureter and the purpose of the stent. If the patient has a stricture or a tortuous ureter, a stiffer or larger-diameter stent is placed if possible. Stents used in guarantees drainage of urine from the kidney into the bladder and bypass any obstruction. Though the actual stone remains, the patient is relieved of chronic pain. Gradually, stents dilate the ureter, making ureteroscopy and other endoscopic surgical procedures easier to perform later. Advantages include:

Stents tend to prevent the rapid dumping of large amounts of stone fragments and debris into the ureter (called steinstrasse).

Stent forces the fragments to pass slowly, which is more efficient and prevents clogging.

However, Stents do have its own drawbacks as well. Stents can become blocked, kinked, dislodged, or infected. A KUB radiograph can be used to determine stent position, and urinalysis can diagnose infection. A renal sonogram can also be used to detect obstruction.

Extracorporeal shockwave lithotripsySWL is the least invasive surgical methods for stone removal. This procedure is used to break the stones in to smaller pieces that may facilitate easy passage. It is especially suitable for stones that are smaller than 2 cm and lodged in the upper or middle calyx. The procedure is carried out under varying degrees of anesthesia (depending on the type of lithotriptor used). The patient is placed on a table and brought into contact with the shock head. The deeper the anesthesia the better the results obtained. Evidence shows that slower shockwave delivery (60-80 per min) gives better results. New lithotriptors comes with 2 shock heads, which deliver a synchronous or asynchronous pair of shocks (possibly increasing efficacy), have attracted great interest.

The shock head delivers shockwaves developed from an electrohydraulic, electromagnetic, or piezoelectric source. The shockwaves are focused on the calculus, and the energy released as the shockwave impacts the stone produces fragmentation. The resulting small fragments pass in the urine.

However, SWL cannot be used if the size of the stone is larger or the stone is located in the lower section of the kidney. Though fragmentation occurs, the results obtained are not optimal.

Percutaneous nephrostomyPercutaneous nephrostomy is an interventional procedure used when drainage of an obstructed kidney is necessary and stent placement is inadvisable or impossible. It is most useful for patients where stent placement may aggravate infection by pushing infected urinary material into the obstructed renal unit.

A needle and then a wire, over which is passed a hollow sheath, are inserted directly into the kidney through the skin of the flank. Percutaneous access to the kidney typically involves a sheath with a 1-cm lumen, which will admit relatively large endoscopes with powerful and effective lithotrites that can rapidly fragment and remove large stone volumes. Renal calyces, pelvis, and proximal ureter can be examined and stones extracted with or without prior fragmentation.

In some cases, a combination of SWL and a percutaneous technique is necessary to completely remove all stone material from a kidney. This technique, called sandwich therapy, is reserved for staghorn or other complicated stone cases. In such cases, experience has shown that the final procedure should be percutaneous nephrostolithotomy.

Open nephrostomySince the development of SWL and endoscopic and percutaneous techniques, open nephrostomy has been used less. It constitutes less than 1% of all interventions. Disadvantages include longer hospitalization, longer convalescence, and increased requirements for blood transfusion.

ChemoprophylaxisPreventive measure might include limitation of dietary components, addition of stone-formation inhibitors or intestinal calcium binders, and increase in fluid intake. Patients should be advised to avoid excessive salt and protein intake.

Chemoprophylaxis of uric acid and cystine calculi consists primarily of long-term alkalinization of urine. If hyperuricosuria or hyperuricemia is documented in patients with pure uric acid stones (present in only a relative minority), allopurinol (300 mg qd) is recommended because it reduces uric acid excretion. Pharmaceuticals that can bind free cystine in the urine (eg, D-penicillamine, 2-alpha-mercaptopropionyl-glycine) help reduce stone formation in cystinuria. Therapy should also include long-term urinary alkalinization and aggressive fluid intake.

Dietary Measures Increase in the fluid intake to increase the volume of urine output is the single most important aspect of stone prophylaxis. Patients with recurrent nephrolithiasis are instructed to drink 8 glasses of fluid daily to maintain adequate hydration and decrease chance of urinary supersaturation with stone-forming salts. The goal is a total urine volume in 24 hours in excess of 2 liters. Another important aspect of dietary measure involves avoidance of excessive salt and protein intake. Calcium should be moderately taken as complete elimination is not advisable. Reducing dietary calcium in these patients may actually worsen their stone disease, because more oxalate is absorbed from the GI tract in the absence of sufficient intestinal calcium to bind with it. An empiric restriction of dietary calcium may also adversely affect bone mineralization and may have osteoporosis implications, especially in women. This practice should be condemned unless indicated based on a metabolic evaluation. As a rule, dietary calcium should be restricted to 600-800 mg/d in patients with diet-responsive hypercalciuria who form calcium stones. This is roughly equivalent to a single high-calcium or dairy meal per day.

Prevention of Nephrolithiasis The most common causes of kidney stones are hypercalciuria, hyperuricosuria, hyperoxaluria, hypocitraturia, and low urinary volume. Each of these major factors can be measured easily with a 24-hour urine sample using one of several commercial laboratory packages now available. Kidney stone preventive therapy consists of dietary adjustments, nutritional supplements, medications, or combinations of these. Patients who have a stone at a young age (ie, < 25 y), multiple recurrences, a solitary functioning kidney, or a history of prior kidney stone surgery, a 24-hour urine collection for stone prevention analysis is recommended.